Author + information
- Mohamed Abdel-Wahab1,
- Azeem Latib2,
- Patrick Goleski3,
- Abdelhakim Allali4,
- Eric Horlick5,
- Luca Testa6,
- Malek Kass7,
- Creighton Don3,
- Matheus Simonato dos Santos8,
- John Webb9 and
- Danny Dvir9
- 1Heart Center, Segeberger Kliniken, Bad Segeberg, Germany
- 2Interventional Cardiology Institute San Raffaele Hospital, Milan, Milan, Italy
- 3University of Washington, Seattle, Washington, United States
- 4Heart Center, Segeberger Kliniken GmbH, Bad Segeberg, Germany
- 5University of Toronto, Toronto, Ontario, Canada
- 6IRCCS Policlinico San Donato, San Donato Milanese, Milan, Italy
- 7SBGH, Winnipeg, Manitoba, Canada
- 8Federal University of Sao Paulo, Sao Paulo, São Paulo, Brazil
- 9Centre for Heart Valve Innovation, St. Paul's and Vancouver General Hospital, Vancouver, British Columbia, Canada
Limited data exists on clinical valve thrombosis after transcatheter aortic valve-in-valve (ViV) implantation. Our objective was to determine the incidence, timing, clinical characteristics and treatment outcomes of patients diagnosed with clinical ViV thrombosis.
This is a prospectively collected data from a multicenter database. Centers participating in the Valve-in-Valve International Data (VIVID) Registry were surveyed for thrombosis cases. The following criteria were used to define clinical valve thrombosis: 1) new valve dysfunction (mean gradient > 20 mmHg or increase in mean gradient by >50% from baseline or more than mild transvalvular AR) responding to anticoagulant therapy with complete or partial resolution of the abnormality; and 2) imaging evidence (echo, CT or both) of prosthetic valve thrombosis in the absence of clinical signs of infection. Definite valve thrombosis was diagnosed if both criteria were met, while probable valve thrombosis was diagnosed if only one criterion was identified.
During the study period, 302 ViV TAVIs were performed. Incidence of clinical valve thrombosis was 7.6% (n=23; 12 definite and 11 probable). The median time to detection was 101 days (IQR 21-226). In 7 (30%) patients, THV thrombosis was diagnosed within 30 days after ViV. 15 (65%) patients had worsening symptoms at the time of diagnosis. Mean gradients were elevated in 21 (91%) patients. The mean gradient and the mean aortic valve area at diagnosis were 35 ± 14 mmHg and 0.9 ± 0.3 cm2. Other findings included thrombotic leaflet mass (n=7), leaflet thickening (n=6) and reduced mobility (n = 6). Mean aortic gradient decreased during treatment with anticoagulants (16±6 mmHg at follow-up echo, p<0.001). There were no deaths or strokes related to valve thrombosis. Of the 23 detected cases of valve thrombosis, 13 had balloon-expandable and 10 had self-expanding valves. Valve thrombosis was more common in patients discharged on antiplatelet therapy (11.1% on antiplatelet therapy vs. 1% on oral anticoagulants, p=0.001) and in patients initially treated with either Mosaic or Hancock II bioprostheses (12.9% Mosaic/Hancock II vs. 5.1% all others, p=0.01). The incidence of thrombosis in patients treated with ViV for degenerated Mosaic/Hancock II valves discharged on antiplatelets was 20.7%.
Clinical valve thrombosis after transcatheter ViV implantation for degenerated bioprosthetic aortic valves is common and characterized by imaging abnormalities and increased gradients, and can be effectively treated with oral anticoagulation. It should be ruled-out in patients with elevated post-procedural gradients after ViV TAVI. The high incidence observed after treatment of specific surgical valve types may warrant specific adjustment of the adjunctive antithrombotic therapy.
STRUCTURAL: Valvular Disease: Aortic